Influenza virus A(H1N1)pdm09 hemagglutinin polymorphism and associated disease in southern Germany during the 2010/11 influenza season.
Identifieur interne : 000206 ( Main/Corpus ); précédent : 000205; suivant : 000207Influenza virus A(H1N1)pdm09 hemagglutinin polymorphism and associated disease in southern Germany during the 2010/11 influenza season.
Auteurs : Valeria Falcone ; Sibylle Bierbaum ; Winfried Kern ; Udo Kontny ; Hartmut Bertz ; Daniela Huzly ; Marcus PanningSource :
- Archives of virology [ 1432-8798 ] ; 2013.
English descriptors
- KwdEn :
- Adolescent (MeSH), Adult (MeSH), Aged (MeSH), Base Sequence (MeSH), Child (MeSH), Child, Preschool (MeSH), Evolution, Molecular (MeSH), Female (MeSH), Germany (epidemiology), Hemagglutinin Glycoproteins, Influenza Virus (genetics), Humans (MeSH), Infant (MeSH), Infant, Newborn (MeSH), Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza, Human (epidemiology), Influenza, Human (virology), Male (MeSH), Middle Aged (MeSH), Molecular Sequence Data (MeSH), Multiplex Polymerase Chain Reaction (MeSH), Phylogeny (MeSH), Point Mutation (genetics), Real-Time Polymerase Chain Reaction (MeSH), Sequence Analysis, DNA (MeSH), Severity of Illness Index (MeSH), Young Adult (MeSH).
- MESH :
- chemical , genetics : Hemagglutinin Glycoproteins, Influenza Virus.
- geographic , epidemiology : Germany.
- epidemiology : Influenza, Human.
- genetics : Influenza A Virus, H1N1 Subtype, Point Mutation.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- virology : Influenza, Human.
- Adolescent, Adult, Aged, Base Sequence, Child, Child, Preschool, Evolution, Molecular, Female, Humans, Infant, Infant, Newborn, Male, Middle Aged, Molecular Sequence Data, Multiplex Polymerase Chain Reaction, Phylogeny, Real-Time Polymerase Chain Reaction, Sequence Analysis, DNA, Severity of Illness Index, Young Adult.
Abstract
A novel influenza A virus emerged in early 2009 to cause the first influenza pandemic of the 21(st) century. Understanding the evolution of influenza virus is crucial to determine pathogenesis, vaccine efficacy, and resistance to antiviral drugs. In this study, we investigated the molecular evolution of influenza virus A(H1N1)pdm09 in the 2010/11 influenza season in southern Germany by sequence analysis of the influenza virus hemagglutinin gene from 25 patients with mild, moderate, and severe disease. Phylogenetic analysis revealed co-circulation of different genetic groups. The D222G mutation, which had previously been observed in severe cases, was not detected. Immunocompromised patients were not affected more severely than non-immunocompromised patients (p>0.05), although longer shedding was observed in some of them. Interestingly, additional mutations and potential glycosylation sites were detected in samples from the lower respiratory tract in two patients, but not in the corresponding upper respiratory tract specimens. The H275Y mutation in the influenza virus neuraminidase gene, known to confer resistance to the neuraminidase inhibitor oseltamivir, was detected in one patient.
DOI: 10.1007/s00705-013-1610-1
PubMed: 23397331
PubMed Central: PMC7087040
Links to Exploration step
pubmed:23397331Le document en format XML
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<front><div type="abstract" xml:lang="en">A novel influenza A virus emerged in early 2009 to cause the first influenza pandemic of the 21(st) century. Understanding the evolution of influenza virus is crucial to determine pathogenesis, vaccine efficacy, and resistance to antiviral drugs. In this study, we investigated the molecular evolution of influenza virus A(H1N1)pdm09 in the 2010/11 influenza season in southern Germany by sequence analysis of the influenza virus hemagglutinin gene from 25 patients with mild, moderate, and severe disease. Phylogenetic analysis revealed co-circulation of different genetic groups. The D222G mutation, which had previously been observed in severe cases, was not detected. Immunocompromised patients were not affected more severely than non-immunocompromised patients (p>0.05), although longer shedding was observed in some of them. Interestingly, additional mutations and potential glycosylation sites were detected in samples from the lower respiratory tract in two patients, but not in the corresponding upper respiratory tract specimens. The H275Y mutation in the influenza virus neuraminidase gene, known to confer resistance to the neuraminidase inhibitor oseltamivir, was detected in one patient.</div>
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